Derm Pathology

INFECTIOUS

Disease Image Agent Description/Distribution Risk Factors/Epidemiology Pathogenesis Lab Tests/Dx Tx

IMPETIGO

Staph Aureus OR Streptococcus

pyogenes

Superficial

Begins as pustule

HONEY-CRUSTED

occurs around face esp around nares

5070% of cases are due to S.

aureus, with the remainder being due

to either S. pyogenes or a

combination of these two organisms

Group B streptococci are associated

with newborn impetigo

predisposing factors: minor trauma,

pre-existing skin disease, poor

hygiene

Streptococci may be early pathogen w/

staphylococci replacing streptococci as

the lesion matures

s. aureus: exotoxins and coagulase

topical tx: bacitracin or mupirocin

be sure to treat around nares to

prevent shedding

BULLOUS

IMPETIGO

Staph Aureus Of all impetigo 30% results in bullous

impetigo.

Blisters occur at site of infection of Group

II phage type 71 Staph aureus

Exfoliative toxins (ETs): act as serine

proteases and can cleave human

desmoglein 1, an adhesion molecule in

the skin -> causes blister and allows

bacteria to spread under the skin -->

Phage typing

FOLLICULITIS

Staph Aureus, pseudomonas

(hot tub folliculitis)

superficial infection of hair follicles:

erythematous follicular-based papules and

pustules

beard, post neck, occipital scalp, axillae

topical treatment with clindamycin 1%

or erythromycin 2%, coupled with an

antibacterial wash or soap

FURUNCULOSIS

Staph Aureus deeper follicular infection: acute, round,

tender, circumscribed, perifollicular

staphylococcal abscess that generally ends

in central suppuration

pustule enlarge --> tender red nodule -->

painful --> RUPTURE --> pain subsides

Systemic anti-staphylococcal

antibiotics

small furuncles: warm compresses

large furuncles/carbuncles: incision

and drainage

MRSA: vancomycin

CARBUNCULOSIS

Staph Aureus coalesced furuncles forming larger

draining nodules, with separate heads.

back of neck, back, thighs

tender, painful, and have fever and

malaise

ECTHYMA

staphylococcal or streptococcal

pyoderma

nearly always of the shins or dorsal feet

begins with a vesicle or vesicopustule,

which enlarges and in a few days becomes

thickly crusted

underlying superficial saucer-shaped ulcer

with a raw base and elevated edges

remains

clean w/ soap and water, abx ointment

ERYSIPELAS

Group A streptococcal infection of the skin involving superficial

dermal lymphatics

local redness, heat, swelling, and a highly

characteristic raised, indurated border

young children and elderly

risk factors: lymphedema, venous

status, DM, trauma, alcoholism,

obesity

B-hemolytic penicillin

CELLULITIS

s. aureus or strep pyogenes infection extending to subcutis

more diffuse w/ ill defined borders and

spreads rapidly

constitutional sx, regional LAD,

sometimes bacteremia

risk factors: lymphedema, venous

status, DM, trauma, alcoholism,

obesit

untreated --> bullous and necrotic -->

abscess/fasciitis

oral Abx: need broad spectrum

parenteral therapy for pts w/ extensive

disesase, systemic sx, or

immunocompromised

good hygiene, warm compresses,

elevate affected limb

BACTERIA

INFECTIOUS

NECROTIZING

FASCIITIS

Microaerophilic -hemolytic

streptococci, hemolytic

staphylococcus, coliforms,

enterococci, Pseudomonas, and

Bacteroides

acute necrotizing infection involving the

fascia and subcutaneous tissue

Within 2448 h, redness, pain, and edema

quickly progress to central patches of

dusky blue discoloration, with or without

serosanguineous blisters

Anesthesia of the involved skin is very

characteristic. By the fourth/fifth day, these

purple areas become gangrenous

w/o tx --> fever, systemic toxicity, organ

failure, shock, death

may follow surgery- perforating

trauma, or may occur de novo

predisposing factors: DM, cirrhosis,

IV drug use

CT or MRI: delineate

extent of infection

biopsy, gram stain,

culture to help identify

organism

early surgical

debridement/fasciotomy, sometimes

amputation

IV abx: gentamicin and clindamicin

supportive care

can still have 70% mortality w/

treatment

BACILLARY

ANGIOMATOSIS

bartonella toxin proliferates endothelium cells

SECONDARY

SYPHILIS

treponema palldium lesions on palms/soles after systemic

infection seeds into skin

acquire virus through inhalation or

exposure of mucous membranes

may go through several rounds of

replication before skin manifestations

virus can stay localized if infect specific

region

exantheums --> virus transmitted via

resp route but not contact w/ rash

MEASLES

(Rubeola)

Measles virus maculopapular lesion

Koplik spots: gray spots on buccal

mucosa

prodrome: cough, conjunctivitis, high

fever

exanthem: hairline, face, neck -->

trunks/extremities

complications: pneumonia, encephalitis,

SSPE

RUBELLA (aka

German

Measles)

prodrome: mild constitutional sx

exanthem similar to measles

posterior cervical and auricular nodes

involved

complications: CONGENITAL rubella

syndrome, teratogenic

ERYTHEMA

INFECTIOSUM

(5th Disease)

Human Parvovirus B19: tiny

naked ssDNA

slapped cheek syndrome

prodrome: mild URI sx

exanthem: slapped chekk --> trunk -->

central clearing

complications: aplastic anemia

ROSEOLA

INFANTUM (6th

Disease)

Human Herpes Virus 6 (HHV6):

large enveloped dsDNA

prodrome: URI sx, abrupt-onset high fever

that breaks

fine macular rash on trunk -->

extremities

complications:pneumonia

VIRUSES

INFECTIOUS

HERPES SIMPLEX

Recurrent HSV-1 is the cause

95% or more of the time

HSV1 = orofacial

HSV2 = genital

most frequent clinical manifestation of

orolabial herpes is the cold sore or fever

blister.

typically presents as grouped blisters on

an erythematous base

HERPES LABIALIS: fever blisters

PRIMARY GENITAL INFECTION: erosive

dermatitis on external genitalia

prodrome: pain, burning, itching

infects mucosal surfaces

HSV multiplies in nucleus and

surroundes themselves w/ nuclear

membrane envelope

HSV1: latent in trigeminal ganglion

HSV2: latent in sacral ganglion

reactivates from psychological or

physical stress

infectious via contact

viral culture: confirms dx

direct fluorescent Ab:

helpful but less specific

Tzanck smear: rapid dx

but less sensitive

acyclovir

HERPES ZOSTER

Reactivation of Varicella Zoster

Virus following primary infeciton

or vaccination

eruption initially presents as papules and

plaques of erythema in the dermatome.

Within hours, the plaques develop blisters

begins w/ pain/paresthesia in band like

pattern

post-herpetic neuralgia: continued pain

after skin disease resolves

dormant in sensory ganglia

reactivates from immunosuppression,

emotional stress/trauma --> dermatomal

dermatitis

start early on prednisone

rest, analgesics, compresses, antiviral

therapy

disseminated/opthalmict ypes --> IV

acyclovir

WARTS

more than 100 types of HPV benign epidermal neoplasm: hyperplasia +

hyperkeratosis

elevated, rounded papules with a rough,

grayish surface

Tiny black dots may be visible,

representing thrombosed, dilated

capillaries

Warts DO NOT have dermatoglyphics

(fingerprint folds), as opposed to calluses

FLAT WARTS = verruca planar

PLANTAR WARTS

Spontaneous resolution (10% stay)

Pare the lesion down: CPT code 11055

Topicals: Salicyclic acid Pads (cut to fit).

Hold on with duct tape; Aldara. Apply

every night (cover with bandaid)

Liquid nitrogen: Location dependant 10-

30sec twice

Persistent treatment (every 2-4 weeks):

Hemorrhagic Blister is Okay (good sign)

Tricks: Forceps and Q-tip

GENITAL WARTS

HPV 6, 11, 16, 18

Risk of cervical cancer with

Type 16, 18

Incubation can be many months

CONDYLOMA ACUMINATUM

MC Viral sexually transmitted

disease

30-50% Sexually Active adults have

HPV

5% clinical sxs

sexually transmitted

direct contact from break in skin -->

wart appears 2-9 mo --> wart disrupt

adjacent skin --> warts spread

infectious via contact

Liquid Nitrogen: Location dependant

usually 10sec

Aldara: Apply every night as tolerated 6-

12weeks

Sometimes every other night

Wash off in the morning

Persistent treatment if needed

Not completely clear

Notify sexual partner(s)

INFECTIOUS

MOLLUSCUM

CONTAGIOSUM

Poxvirus, MCV-1, 2, 3 or 4 smooth-surfaced, firm, dome-shaped,

pearly papules, averaging 35 mm in

diameter may be up to 1.5 cm in diameter

central umbilication with central

keratotic plug

intertriginous sites, axillae, popliteal

fossa, groin

3 groups are primarily affected: young

children, sexually active adults, and

immunosuppressed persons

Virion is encased in a protective sac

transmission from direct skin or mucous

membrane contact

virus replicate in cytoplasm --> induce

hyperplasia

resolve spontaneously but can persist

in immunocompromised pts

infectious via contact: atopic skin,

shaving, bathers, wrestlers, sex

Nothing: 6-8weeks individual; Auto

inoculate up to a year

Liquid nitrogen with q-tip for 5 seconds

Curettage (brutal !) dont use! Leave

scar

Aldara: AAA qd or qod 3-4weeks

Natural habitat is water, soil or decaying

vegetation

Only a few species are pathogenic for

humans.

Cell Membrane and Wall Structure

They are eukaryotic cells.

Cell membrane and wall similar to gram

positive bacteria bc theres a cell

membrane surrounded by a cell wall

Fungal membrane contains ergosterol -

> different than human cell membranes

that have cholesterol

Cell wall from inner most layer-out:

Chitin -> glucan -> mannoproteins

Unlike bacteria it contains no

peptidoglycan.

KOH Preparation

Skin is swabbed with 70%

ETOH and allowed to air

dry

Surface is scraped to

remove skin scales or hair

that contain the fungus

Specimen is treated with

10% potassium hydroxide

to destroy tissue elements,

specifically keratin (thus

KOH is a clearing agent.)

Look for branching

hyphae or yeast cells.

YEAST Unicellular Reproduce by budding. Some also

produce pseudohyphae.

MOLDMulticellular Produce hyphae Solid media: grow as

smooth colonies and look

very much like bacteria

CANDIDIASIS

candida involvement of folds and occurrence of

many small erythematous desquamating

satellite or daughter lesions scattered

along the edges of the larger macules

CANDIDAL INTERTRIGO: intertriginous

areas often affected bc inc warmth,

moisture, and maceration, permitting

organism to thrive --> becomes reddened

plaques

ORAL THRUSH = oropharyngeal

candidiasis: easily scrapable nonadherent

plaques, dysphagia

PARONYCHIA: infection of nail w/ tender,

edematous, erythematous nail folds w/

purulent discharge

CANDIDAL VULVOVAGINITIS: acute

inflammation of the perineum

characterized by itchy, reddish, scaly

vaginal mucosa; and creamy discharge.

BALANITIS: shiny reddish plaques on

glans penis

immunocompromised, diabetes,

elderly, pts on abx

usually on skin flora --> altered host env

leads to proliferation

KOH prep: budding yeast,

pseudohyphae

fluconazole 1x/week, stays in

skin/hair/nails for 6-7 days

no talcum --> irritating

CANDIDA INTERTRIGO, BALANITIS:

topical antifungals (azoles)

THRUSH: nystatin or clotrimazole

PARONYCHIA: topical antifungal 2-3

mo, PO anti-staph abx

VULVOVAGINITIS: fluconazole

FUNGI

SUPERFICIAL MYCOSES

INFECTIOUS

PITYRIASIS

VERSICOLA

Malassezia furfur hypo- or hyperpigmented coalescing scaly

macules on the trunk and upper arms

Heat and humidity

systemic corticosteroid use,

cushing's, immunosuppression,

malnutrition

Dicarboxylic acids inhibit melanin

production by inhibiting tyrosinase -->

hypopigmentation

griseofulvin and lamisil do not work -->

more for dermatophytes

Sold media: produce

filamentous colonies

ALL TINEA

INFECTIONS

Survive on dead keratin

Classified by body region

KOH from scale at border

Get a culture

TINEA NIGRA

Hortae Werneckii dimorphic fungus Strands of mycelium and

numerous spores called

spaghetti and meatballs

when viewed

microscopically (KOH prep)

Wood's light exam

acentuates pigment

changes

BLACK PIEDRA

Piedra hortae

WHITE PIEDRA

Trichosporon beigelii

topical: terbinafine, clotrimazole,

econazole

TINEA PEDIS aka

Athlete's Foot

Trichophyton rubrum

1 T. mentagrophytes

Epidermophyton floccosum

Affected skin is usually pruritic, with scaling

plaques on the soles, extending to the

lateral aspects of the feet and interdigital

spaces often with maceration.

Adolescents and young males

most common fungal infection in

north america and europe

TINEA UNGUIUM

T. rubrum

T. mentagrophytes

thickened yellow nails and hyperkeratotic

subungual debris

TINEA CRURIS

T. rurum

E. floccosum

jock itch: in groin, upper/inner thighs but

spares the groin

scaling annular plaques

common in men

TINEA CORPORISCaused by any dermatophyte Ringworm infection

face, hands, body

Especially in children

TINEA MANUUMT. rubrum infection of palms of hand

ECTOthrix- caused by

Microsporium audouinii,

Microsporium canis and some

trichophyton.

hyphal elements and arthrospores

SURROUND the hair shaft

Hair breaks a few millimeters ABOVE the

scalp

ENDOthrix- caused by

Trichophyton tonsurans

Arthrospores INSIDE the shaft itself

Hair breaks AT the scalp

TINEA BARBAET. mentagrophythes

T. verrucosum

infection of beard hair

infection of : scaly erythematous skin w/

hair less

Topicals:

Powders

Domeboro solution 20min TID

Selenium sulfide for hair

Azoles creams: Some have antibiotic

capabilities (spectazole)

Lamisil or nafitine bid x 2-4weeks

(fungicidal)

Oral

Location (scalp and groin) and size

dependant

Griseofulvin 20-25mg/kg/d divided BID

and Lamisil 2-6weeks

CUTANEOUS MYCOSES

TINEA CAPITIS common children

AUTOIMMUNE/INFLAMMATORY

Disease Image Description/Distribution Risk Pathogenesis Lab Tests/Dx TxWheals, many diff shapes and

sizes Type I hypersensitivity supportive

antihistamines: H1 blockers, H2

blockers, doxepin

steroids: long taper

avoid irritants/allergen

barrier cream: zinc oxide

antihistamines

topical steroids

patch testing

red poorly defined plaques w/

scale and crust on cheeks

associated w/ asthma

and allergic rhinitis

chronic pruritic inflammatory

skin disease MOISTURIZE

infants/toddlers: cheeks,

forehead, EXTENSORS

most common in

developed countries

genetics: fillagrin mutation -->

cause transepidermal water

loss Avoid perfumes, soaps, hot waterolder children/adolescents:

flexural areas of neck, elbows,

wrists, ankles impaired immune response antihistamines

adults: FLEXURAL areas of wrists,

ankles, feet, face

Topical steroids: OINTMENTS

stronger, avoid use in

intertriginous areasdry skin/xerosis

diaper area spared COMPLICATIONS:

Dennie-Morgan lines: double

folds and lines under eyes from

chronic edema

Lichenification: thick callous

skin from chronic trauma

Horizontal nasal crease: from

constantly scratching nose

Neurodermatitis: itch-scratch

cycle, becomes subconscious

from scratching

Scars

Infections: impetigo, warts,

molloscumEczema herpeticum: HSV can

use atopic dermatitis to invade

and spread into skin

comedome (pore) --> oil and

keratin builds up --> ruptures

hair follicle --> bacteria

accumluates --> inflammatory

response --> PUSTULES

Comedomes: topical retinoids,

accutane

Bacteria: Abx, benzoyl peroxide

Inflammation: Abx, benzoyl

peroxide, hormonal therapy,

accutane

Sebum production: hormonal

therapy, accutane

erythematous targetoid lesions

in palms or mucous membranes,

B/L and symmetric

immune complex formation --

> deposit in cutaneous

microvasculature work up: HSV titers, skin biopsy PO prednisone

drugs: sulfonamides,

anticonvulsants

early histologic findings: vacuolar

interface dermatitis, perivascular

lymphocytic infiltrate acyclovir 4x/day

infection: HSV, mycoplasma

idiopathic

from meds: abx, anti-

epileptics, NSAIDs

death rate: 1-5%

initial sx: fever, stinging eyes,

swallowing

true derm emergency --> high

morbidity and poor prognosis

severe, denudation (>30%

epidermal detachment), also

from meds death rate: 34-40% transfer to ICU/burn unit

CONTACT

DERMATITIS

pruritic, erythematous oozing

rash

contact to poison ivy,

nickel, rubber,

preservatives

Type IV hypersensitivty to

IRRITANTS (larger than

Ag/allergens)

URTICARIA

can migratechronic types: still can rarely

find a cause

eosinophils

ERYTHEMA

MULTIFORME20-40 yo

late histologic findings:

subepidermal bullae, full thickness

necrosis

Abx: for skin infections but use

sparingly

ACNE

4 factors: follicular

hyperkertinization, excess

sebum, bacteria, inflammation

ATOPIC DERMATITIS

Pityriasis alba: small

hypopigmented ill-defined

patches on face from inhibition

of melanin due to thicker skin

environment/stress

TOXIC EPIDERMAL

NECROLYSIS

STEVEN JOHNSON

SYNDROME

widespread blisters and purpuric

macules. mucosa involvement

and

< 10% epidermal detachment


great loss of water/fluids -->

need to go to burn unit

steroids controversial: can't fight

off infection

increased risk for infection -->

die from SEPSIS IVIG: best tx but expensive

fat disorder on extensor surfaces

of extremities, more common on

ant shins

hypersensitivity rxn to: URI,

infection, IBD, malignancies,

sulfonamides, Ocs

supportive: NSAIDs,

supersaturated solution of

potassium iodide in orange juice,

PO prednisone

prodrome: fever, joint pain,

malaise

rash occurs for 1-3 wks then

resolves Abx for URI

well demarcated thick

erythematous plaques w/ silver

scale on extensor surfaces clinical

Topical steroids (NOT ORAL):

potent except for intertriginous

areas

PLAQUE: silver scale and sharp

demarcations, symmetric. Most

common type

histology : acanthosis, elongated

rete ridges, hyperkeratosis and

parakeratosis Calcipotrene: Vit D derivative

INVERSE/FLEXURAL: bright red

plaques in skin folds with no

scales (often misdiagnosed as

candidiasis) OTHER FINDINGS:

phototherapy: UVB, excimer laser,

PUVA

GUTTATE: Rain-drop sized salmon-

pink scaly papules on trunk or

extremities. Usually after strep

infection

Psoriatic Arthritis: Sausage

digits, tenosynovitis, affects

DIP joints or sacroiliitis

systemic (for psoriatic arthrits):

MTX, cyclosporine, acitretin

PUSTULAR: Sterile pustules in

cornified layers, on palms and

soles. Often from withdrawal of

corticosteroids --> AVOID ORAL

STEROIDS FOR PSORIASIS

Nail changes: Pitting, oil

spots, onychodystrophy

Biologics: TNF-a inhibitor, IL 12/23

blocker

Scalp involvement

Geographic tongue: Plaque

psoriasis on tongue, may have

bad breath

high risk for CVD

purple, pruritic polygonal

papules

widespread papulosquamous

eruption

Flaccid blisters and erosions w/

frequent mucous involvement

IgG against Dsg 3 --> lose

normal adhesion histology:

Nikolsky sign: intact epidermis

shearing away from dermis -->

leave moist surface behind suprabasilar acantholysis

intraepidermal bullae

blisters/separates within epidermal

layer

tombstone row of basal layer

keratinocytes

immunofluorescence: chicken

wire/fish net pattern

Flaccid bullae and localized or

generalized exfolication, rapidly

denudes

intact bullae, erythematous

papules, urticarial plaques

involving skin and mucosa

histology: Subepidermal bulla with

eosinophils or neutrophils

can be in groin, axillae, trunk,

thighs immunofluorescence: linear

TOXIC EPIDERMAL

NECROLYSIS Nikolsky's sign: lateral pressure

induce separation of epidermis

from dermis

Auspitz sign: pinpoint bleeding

after picking off scale, from vessels

in dermal papillae

LICHEN PLANUS

histology: hyperkeratosis,

acanthosis, saw-tooth elongation

of rete ridges, lymphocytic

infiltrate

ERYTHEMA

NODOSUM

PSORIASIS

ERYTHRODERMIC: Bright red

lesions involving full body w/

fevers/chills/malaise. Often from

uncontrolled or untreated

psoriasis --> need hospitalization

T cell mediated: releaseTNF-

and interleukin cytokines

body starts to produce skin at

faster rate

histology: acanthosis,

hyperkaratosis, hypergranulosis,

elongated rete ridges, fibrosis of

papillary dermis

PEMPHIGUS

VULGARISAsboe-Hansen sign: put pressure

on intact bullae fluid spreads

under adjacent skin and makes

blister bigger

40-60 yo, M = F

intralesional kenalog injections

LICHEN SIMPLEX

CHRONICUS

from repetitive

trauma/scratching

BULLOUS

PEMPHIGOID60-80 yo, M=F

IgG against basement

membrane /hemidesmosomes

(BP230, BP180)

PEMPHIGUS

FOLIACEUS

face, scalp, upper trunk

middle aged and

elderlyIgG against Dsg 1 histology: Subcorneal acantholysis


Associated w/ gluten-

sensitive enteropathy

HLA-B8, HLA-DR3, HLA-DQw2 Type III hypersensitivity:

granular IgA in papillary

dermal tips

non-scarring alopecia/balding in

round defined area

hair specific autoimmune

disease no tx: 90% clear within one year

asymptomatic: no scale,

erythema, orLAD

Lymphocytic infiltrates

sometimes around or within

hair bulb of anagen follicles Minoxidil (rogaine)

Topical steroids: if autoimmune, <

10 yo

intralesional steroid injections

foreign body inflammatory rxn

to dark coarse curly hair stop shavingshaving --> hair curls and dives

back into skin --> brings in

bacteria use single blade/electric razor

retin-A: decrease hyperkeratosis

topical corticosteroids

oral or topical abx: for

pustules/abscesses and reduce

skin bacteria

laser hair removal: painful and

only works short-term

pustular --> short-course of abx

hyperkeratosis --> retin-A gel, high

potency topical steroids

scar --> intralesional steroids TAC

excision in stages

ALOPECIA AREATA

regrown hair can be white can be stress induced

DERMATITIS

HERPETIFORMIS

Intensely pruritic papulovesicular

eruption symmetrically on

elbows, knees, buttocks

20-60 yo, maleshistology: neutrophils in

subepidermal space

ACNE KELOIDALIS

NUCHAEchronic scarring folliculitis

chronic irritation: close

haircuts, rubbing of head gear

PSEUDOFOLLICULITIS

BARBAE

transfollicular or extrafollicular

penetration of foreign bodies

bumps proliferate with more

shaving

SYSTEMIC/CONNECTIVE TISSUE DISEASES

Disease Image Description/Distribution Pathogenesis Lab Tests/Dx Tx

systemic disease involving skin

(malar rash, discoid rash), oral

ulcers, heart, kidneys, joints, neuro,

blood

type III hypersensitivity

Anti Ro/La (ssDNA) sun avoidance

suspect if have frequent miscarriages

cell rupture releases

"garbage" DNA -->

macrophages can't clear

completely --> Ab made

against DNA/histone

proteins --> complexes

deposit throughout body

ANA: main screening test --

> 1:160 = positive. but have

false positives (infection,

elderly, pregnant) topical steroids

ACUTE CUTANEOUS LE form: looks

like SLE, photodistributed butterfly

rash. No internal involvement

need 4 of 11 criteria: malar

rash, discoid rash,

photosensitivity, oral

ulcers, arthritis, serositis,

renal disorder, neuro

disorder, hematologic

disorder, immunologic

disorder, antinuclear Ab

plaquenil: dec immune

system and reduce sun

sensitivity but need optho

exam before starting

SUBACUTE LE: photodistributed

annular plaques, joint and vasculitis

involvementwork up: blood work,

biopsy IL kenalog

CHRONIC/DISCOID LE:

photosensitivity atrophic plaques on

scalp --> scarring alopecia. Rarely

ANA positiveimmunosuppressants:

Imuran, MTX

NEONATAL LUPUS: mother pass Ab to

kids --> kids get anti-Ro and heart

block

DRUG INDUCED LE: from hydralazine,

procainamide, isoniazid

proximal muscle weakness with

cutaneous manifestation

Ab tests: ANA, Jo-A, SS-A

(ro), t-RNA synthetase topical steroids

adult variant: associated w/ internal

malignancy --> SCREEN for cancers

muscle biopsy = gold

standard LOTS of oral prednisone

child variant: calcinosis of skinadd steroid sparing agent

w/in 2 months: MTX, imuran,

celicept

heliotrope rash avoid sun

Gottron's papules: raised fleshy

colored lesions plaquenilperiungual erythema and

telangiectasia: capillary loops in

proximal nail bed thrombose/break shawl sign: violaceous scaling

patches around shoulder

diffuse, hard immobile skin

chronic fibrosing systemic

disease --> fibroblasts

activated to make more

collagen MTX

SYSTEMIC SCLEROSIS: diffuse and

CREST syndrome (calcinosis,

raynaud's, esophageal involvement,

sclerodactyly, telangiectasia)

systemic fibrosis: have resp

(interstitial fibrosis,

pulmonary HTN), CV, GI,

kidney issues. Most die from

renal HTN diffuse: anti-scl70

Raynaud's --> calcium

channel blocker

penicillamine

ACE: renal protection

morphea tx: IL Ken at leading

age, topical CS, plaquenil

non-blanchable spots on trunks/legs

that are raised --> palpable purpura punch biopsy PO steroids and refer to derm

GIANT CELL/TEMPORAL

ARTERITIS U/L headache near temples

need to dx quickly or else

may turn BLINDbiopsy temporal artery HIGH DOSES of PO steroids

pulseless disease: fever arthritis,

weak pulses in extremities

CONNECTIVE TISSUE DISEASES

SLE

VASCULITIS

TAKAYASU ARTERITIS

DERMATOMYOSITIS

SCLERODERMA

LOCALIZED SCLEROSIS: morphea -->

just involves skin. atrophic plaques

(skin steps off) w/ telangiectasia.

Middle aged females

limited: anti-centromere


young asian females

affects renal and visceral

med-sized vessels

associated w/ HBV

in children

HIGH FEVERS

red conjunctiva

circumoral palor

red perianal rash

lymphadenitis

peripheral desquamationgranulomatous inflammation

of resp tract C-ANCA (anti-pr3) positive steroids + cyclophosphamide

nasopharynx, lung, kidney

involvement

necrotizing vasculitis of small-

med sized vessels CXR: migratory infiltrates

second line: IVIG, cellcept,

rituximab, azathioprine

saddle nose deformities necrotizing

glomerulonephritis UA: RBC/casts fatal if not tx aggressively

friable erythematous gingiva:

strawberry mouth

triggers: vaccine, LT-

inhibitors, cocaine,

azithromycin, rapid stop of

steroidsP-ANCA (anti-MPO)

positive steroids

lung and heart involvement

eosinophil-rich and

granulomatous inflammation

of resp tract

CBC: peripheral

eosinophilia

cytoxan: if have cardiac

disease

necrotizing vasculitis of small-

med sized vessels

heart disease = most

common cause of death

SQ nodules: may ulceratenecrotizing vasculitis of small

vessels steroids 1 mg/kg/day to start

lung and kidney involvementnecrotizing

glomerulonephritis

cyclophosphamide or

azathioprine: for severe renal

or lung disease

prodrome: fever, arthalgia, myalgia,

weight losspulmonary capillaritis

IVIG

splinter hemorrhages, ulcers,

necrotizing livedo

type III hypersensitivity: IgA

dominant immune deposits

in small vesselsneed serial UA to track

kidney function self-limited

affects kids

IF: IgA, C3 and fibrin

deposition in affected

vessel walls

Dapsone, Colchicine: dec

duration of cutaneous lesions

skin, gut, kidney involvement systemic corticsteroids: for

arthrlagias and abd pain

palpable purpura in lower extremities

refer to nephrologist

headache, joint pain (LE large joints),

hematuria, rash, abdominal pain

waste basket dx

CRYOGLOBULINEMIC

VASCULITIS

no signs of systemic disease or

glomerulonephritis

cryoglobulin immune

deposits in skin and

glomeruli --> precipitate out

w/ cold and occlude blood

vessels

congenital capillary

malformation: deficiency of

SNS innervation of vessels

color gets dark w/ crying,

fever, overheating

in < 1% of newbornscan evolve to raised,

thickened plaque

TAKAYASU ARTERITIS

POLYARTERITIS

NODOSAbelly pain, skin erruption

PO steroids,

cyclophosphamides

KAWASAKI DISEASEcan get coronary artery

aneurymsIVIG, ASA, PO steroids

MICROSCOPIC

POLYANGIITIS

HENOCH-SCHONLEIN

PURPURA

P-ANCA positive

preceded by URI strep or

other infectious triggersusually clincial dx

WEGNERS

GRANULOMATOSIS

CHURG-STRAUSS

SYNDROME

associated allergic rhinitis, nasal

polyps, asthma

CUTANEOUS MANIFESTATIONS OF INTERNAL DISEASE

LEUKOCYTOCLASTIC

VASCULITISfrom drugs, URI

NEVUS FLAMMEUS

port wine stain in head and neck:

dermatomal, unilateral, variable

blanching


ACANTHOSIS

NIGRICANS velvety hyperpigmented plaque

Nonspecific reaction pattern

that may accompany

obesity; diabetes; excess

corticosteroids; pineal

tumors; other endocrine

disorders

determine type of

xanthoma

measure fasting

cholesterol, TAGs, HDL,

VLDL, LDL

primary

hyperlipoproteinemia = dx

of exclusion

congenital lesions of skin, CNS, bone,

endocrine glands

autosomal dominant

congenital disease > 2 or more features = NF1

dx excise cutaneous tumors

> 6 caf au lait spots NF1 gene MRI: dx, management, and

screening of family

members

follow pt closely to detect

malignant degeneration of

neurofibromas

axillary freckling: earliest sign

genetic counseling

cutaneous neurofibromas

Lisch nodules: iris hamartomas

bone lesion: sphenoid wing

dysplasia or congenital bowing of

long bones

bilateral acoustic neuroma autosomal dominant

1-2 caf au lait spots

neurofibromas: less common than

NF1

no lisch nodules or mental

retardation/learning disabilities

caf au lait, low set ear, webbed neck

short stature, pectus excavata

pulmonic stenosis, cryptorchidism,

hypogonadism

short, facies, low set ears

caf au lait, cardiac defects

large segmental caf au lait sporadic: GNAS1 mutation

bone lesions: polyostotic fibrous

dysplasia

precocious puberty,

hyperthyroidism

caf noir spots: more black than

creamy

XANTHOMASbuild-up of lipids in tissue due to

dyslipidemialipid abnormalities

NEUROFIBROMATOSIS

1

NF1 + juvenille

xanthogranuloma = HUGE

risk of juvenille CML

NEUROFIBROMATOSIS

2 SCH gene:

swannomin/merlin proteins

defective

MCCUNE ALBRIGHT

SYNDROME

NOONAN SYNDROMEautosomal dominant:

PTPN11 mutation

CARDIOFACIOCUTANEOU

S SYNDROME

BRAF, MEK1, MEK2

mutations

LEOPARD SYNDROME PTPN11 mutation


EKG conduction defects, deafness,

hypospadias/cryptorchidsm

Multiple hamartomas (benign

tumors) of the skin, central nervous

system, kidneys, heart, retina, and

other organs

autosomal dominant

MRI brain genetic counseling

epilepsy + angiofibromas + mental

retardationTSC1, TSC2 gene defect

surgical excision of facial

lesion if cosmetic concern

adenoma sebaceum inc chance of malignancy

shagreen patch: usually in lower

trunks

white ash leaf macules:

hypopigmented ellipitic macule.

Earliest finding

periungual fibromas: tumors around

nails that look like warts

brain lesions: glioneuronal

hamartoma --> cause seizures,

cognitive defects, autism, behavioral

problems

heart: cardiac rhabdomyoma

renal: angiomyolipoma, renal cell

carcinoma

opthalmic: retinal hamartoma

pulmonary:

lymphangioleiomyomatosis --> SOB

and PTX

multiple hamartoma syndromeautosomal dominant: PTEN

mutation

multiple facial trichilemmomas:

looks like wart

oral mucosal papillomatosis

< 10% have caf au lait spotssebaceous gland tumor + > 1

internal malignancy

FAP + extraintestional manifestations

intestinal polyposis, epidermal cysts,

multiple osteomas, desmoid tumors

epidermal cysts on weird locations

(legs)

fibrofolliculomas, achrochordons,

trichodiscomas

LEOPARD SYNDROME PTPN11 mutation

TUBEROUS SCLEROSIS

COWDEN DISEASEhigh incidence of malignant

tumors of breast and/or

thyroid gland

MUIR-TORRE

SYNDROME most common associated neoplasm =

colorectal cancer

autosomal dominant

BIRT-HOGG-DUBE

SYNDROME can get spontaneous PTX and renal

cancers

autosomal dominant

GARDNER SYNDROME

BENIGN LESIONS

Disease Image Description/Distribution Pathogenesis Lab Tests/Dx Tx

benign neoplasm of melanocytes histology: MATURE

melanocytes descending

into dermis

JUNCTIONAL NEVUS (A): flat, at

epidermal/dermal junction

INTRADERMAL NEVIS (C): indurated,

in dermis w/ no connection to

epidermis

COMPOUND NEVUS (B): still

connected to epidermis but growing

down into dermis

brown pigmented lesion w/ hair

present at birth --> monitor carefully

b/c can become melanoma if large

BECKER'S NEVUS: common on men in

lateral upper chest. Lots of hair

associated

HALO NEVI immune rxn against mole from body can get vitiligo

benign juvenille melanoma: most

common in children

hairless, red/brown dome-shaped

papule

slightly elevated, round, regular

nevus

pigment in dermis --> reflects blue

light

LABIAL MELANOTIC

MACULEfaint black spot on lower lip/mucosa

histology: atypical

melanocytes w/ bridging of

rete ridges

cutaneous hamartoma: contains

surface epidermis and adnexal

structures (sebaceous gland)

linear, unilateral, wart-like, whorled

follow Blashkos lines: where

melanocytes travel in utero

ILVEN (inflammatory linear verrucous

epidermal nevus): intensely

erythematous, pruritic, inflammatory

usually scalp present at birth

CONGENITAL NEVUS

serial excisions for

prophylaxis before

turns into melanoma

MELANOCYTIC NEVUS

BLUE NEVUS

SPITZ NEVUS remove

DYSPLASTIC NEVUS

irregular pigmented macule w/

irregular border, smaller than

melanoma

marker for inc risk for

developing melanoma

remove mod and

severe-graded atypia

EPIDERMAL NEVUS present at birth cryo, surgery, laser

NEVUS SEBACEOUS

BENIGN LESIONS

tumors can arise on top:

need prophylactic surgical

excision

common benign neoplasm

= trichoblastoma

common malignancy =

BCC

raised discolored plaques on

extremities or face w/ "stuck on"

appearance genetic predisposition:

rare if < 30 histology: horn cysts shave removal

benign squamous proliferationsign of skin maturity -->

usually in elderly

well-circumscribed,

crumbles when picked curettage

doesn't occur on lips, palms, solesraised and brown = okay,

flat and black = problem

liquid nitrogen: be

careful on dark skin --

> can leave

hypopigmentation

IRRRITATED SK: often confused w/

BCC due to inflamed/swollen look

LESER-TRELAT SIGN: eruptive SK as

sign of internal malignancy (usually

gastric cancer)

STUCCO KERATOSES: papular warty

lesions on lower legs, sign of dry skin

DERMATOSIS PAPULOSA NIGRA:

multiple brown-black papules on

african-americans. "morgan

freeman" disease

silicone gel sheeting:

doesn't work

BCC MIMICS

NEVUS SEBACEOUS linear --> cobblestoned

SYRINGOMA

multiple flesh-colored small papules

around eyes, from eccrine glands

around eyes

histology: comma-shaped

groups of epithelial cells

TRICHOEPITHELIOMA small flesh-colored papules on facehistology: pseudo-horn

cysts

CYLINDROMAflesh-colored to reddish nodule on

head, neck, scalp

turban tumor =

autosomal dominant histology: jigsaw-puzzle

pattern

PILOMATRICOMAfirm nodule in a child w/

erythematous surface

histology: basaloid cell nest,

ghost cells (no nucleus),

giant cells, bone cells and

calcifications

KELOIDSscar that proliferates beyond margin

of injury

SEBORRHEIC

KERATOSIS

tender, itches, grows fast

BENIGN LESIONS

intralesional steroid

injections: large

needle to inhibit

collagen synthesis

more common in blacks

cryotherapy,

compression,

irradiation

invagination of epidermis w/ black

punctum, very common

pore from old hair follicle

invaginates into skin and

grows keratin --> bacteria

makes abscess around it

drain fluctant and

inflamed cysts

commonly on scrotumspontaneously ruptures --

> need to destroy cyst wall

to prevent recurrence

PILLAR CYST: form of EIC without

punctum, on scalp. Filled w/ hard

debrismultiple EICs: suspect

Gardner's syndorme

snip excision w/ iris

scissors

large tag --> shave

removal

cryotherapy: spray or

forceps

surgical excision

cryo doesn't work

asymptomatic to slightly itchy lesions more in females

dimple sign: lesion retract

beneath skin when you

compress and elevate w/

thumb and index finger

fibrous rxn to trauma, viral

infection, insect bite

multiple DFs seen in SLE

inflamed cartilagewomen: antihelix LN2

cut out cartilage

donut pillow: relieve

KELOIDSscar that proliferates beyond margin

of injury

tender, itches, grows fast

EPIDERMAL

INCLUSION CYSTS

small punch biopsy

over black punctum

ACROCHORDONskin tags: tiny, brown/skin colored

and attached by short narrow stalk

from chronic irritation,

rubbing, genetics, obesity

CUTANEOUS HORNhard conical projection made of

keratin

a wart, actinic keratosis,

or SCC

excision: ellipitical or

punch, depending on

size

CHRONDRODERMATITI

S NODULARIS HELICISpain out of proportion if suspect AK men: helix

DERMATOFIBROMA

pinkish papule w/ darker

hyperpigmented ring, usually on leg

MALIGNANT LESIONS

DiseaseImage Subtypes Description/Distribution Risk Factors/Epidemiology Pathogenesis Lab Tests/Dx Tx

malignant neoplasm of

melanocytes personal history of

atypical moles, fam hx

congenital nevus

nonmelanoma skin cancer

immunosuppression

sunburn, PUVA, chronic

tanning, white skinned

UVA >> UVB

Growth Phases

Radial growth: superficial

and laterally

Vertical growth: deeper into

dermis

Pathogenesis

familial melanoma: CDKN2A

mutation --> Rb and p53

inactive

MC1-R gene: increases risk

Better Prognosis factors

young age

female

extremities

skin metastasis better than

visceral

ABCDE

asymmetry, border

irregularity, color, diameter

Color: dark, brown, or pale

Metabolic Panel

+S100

HMB45

Melan A

Histology

Atypical cells in epidermis

Lack of maturation with

descent

Cytologic atypia & nuclear

pleomorphism

Nucleolar variability: often

large & irregular

Mitoses: deep dermal, often

atypical

Increased apoptosis

biopsy depth > 1 mm: need

sentinel LN biopsy

LN pos = metastatic -->

dissect sentinel and

surrounding LN

LN neg: remove primary

tumor

EXCISION

in situ: 0.5 cm margin

< 1 mm: 1 cm margin down

to fascia

> 2 mm: 2 cm margin down

to fascia

Adjuvant Therapy

IFN-a: inc survival but not

well tolerated

Metastatic disease

CT: chest, abd, pelvis

MRI brain

radiation

Breslow Depth

obtain skin biopsy for dx and

staging

predicts survival and

prognosis

measures top of granular

layer to deepest point of

invasion

< 6mm: benign

> 0.76mm DEEP -> regional

lymph node involvement so inc Melanoma in Situ histology: atypical

melanocytes but basement

membrane still intact

Superficial Spread lower leg in female

back/trunk in males

In early states it may be small,

then growth becomes irregular

horizontal superficial spread

w/o much induration

MC type of MM in the

white-skinned population

70% of cases

begins as flat lesion

can turn black, blue, red,

white

Nodular Trunk is a common site

Usually with a POOR prognosis

Black/brown nodule

Ulceration and bleeding are

common

M>F rapid growth

vertical growth phase

MELANOMA

MALIGNANT LESIONS

Lentigo Maligna

Melanoma

Mainly on face in elderly pt

grows on epidermal-dermal

junction

Elderly pts May be many years before

an invasive nodule develops

grows on sun damaged skin

Acral Lentiginous

Melanoma

Usually comprises a FLAT

lentiginous area w. INVASIVE

nodular component

POOR prognosis b/c usually

identified too late --> on palms

or soles

Common in black people

and Asian

In white-skinned

population accounting for

10% of MM

KIT gene: overexpressed.

possible gene association

hutchinson's sign: pigment

spreads under nail plate to

proximal and lateral nail folds

Subungal Melanoma Often diagnosed late

Confusion with benign

subungal nevus, infections or

trauma

Rare

Amelanocytic Melanoma fleshy pink, indurated lesion

Diagnosis is often missed

clinically so do bx

often mistaken for BCC or

verruca

Lack of pigmentation due to

the rapid growth of tumor and

differentiation of the

malignant melanocytes

Desmoplastic

Melanoma

Usually found on head and

neck region

Usually amelanotic lesions

High chance for recurrence

Positive S-100 protein but are

often negative to tyrosinase,

Melan-A.

Conjunctival Melanoma Markedly pigmented tumor in

eye

Metastatic Melanoma Satellitosis near the primary

melanoma

Sometimes distant metastases

that appear as papules or

plaques, not pigmented.

MELANOMA

MALIGNANT LESIONS

Malignant Melanoma Invasive and may show lymph

node invasion by tumor cells

(pics on right)

Rate of Metastasis

pTis (in situ): 5 mm margin

pT1 (4.0 mm): 2

cm margin

Derived from basal cell layer

of epidermis

Head & neck of elderly

patients

Slow, progressive growth

Locally destructive, recurs,

rarely metastasizes

translucent, "pearly" nodule

w/ telangiectasia

high risk: micronodular,

infiltrative, morpheaform,

pigmented types

MC type of skin CA

fair skin, blue eyes, fair

hair

Inability to tan

Exposure to UV radiation

from sunlight or artificial

tanning lamps

UV exposure pattern-

intermittent, childhood sun

exposure

immunosuppression

PTCH mutation: unchecked

cell proliferation

photocarcinogenesis: DNA

damaged by UVB, ROS induces

DNA damage, cell-mediated

immunity suppressed, p53

mutates

p53 mutation: can't trigger

apoptosis

indolent, low metastatic

potential

When washing face, crust

comes off and lesion starts

bleeding

Almost always epidermal

attachment

Nests or lobules of

hyperchromatic but uniform

basaloid cells with PERIPHERAL

PALISADING surrounded by

loose stroma

CLEFT-LIKE retraction spaces

May appear pigmented due

to dermal melanophages

New drug target PATCH

called Vismodegib

ELECTRODESICCATION AND

CURETTAGE (ED&C): great for

small low risk BCC

Excision: large low risk (5

mm) or any high risk (10 mm)

MOHS micrographic surgery:

microscopically controlled

technique with real-time

frozen tissue secitons to

insure margin control; for high

risk, large low risk, face, scalp,

and neck, recurence

Radiation- adjunctive

therapy if can't do surgery, or

if have perineural invasion

Aldara- low cure rate

Nodular BCC low risk

Superficial BCC Erythematous plaques w/ +/-

papules, scale, telangiectasia

low risk

Morpheaform BCC scar-like or white plaque w/

slight translucence. Looks like

scar on nose

high risk

Cystic BCC well-marginated, red or flesh-

coloured nodule with cystic

centers. POPPING DOES NOT

RESOLVE IT --> not just a simple

cyst

Fibroepithelioma of

Pinkus

smooth pink plaque on lower

back. Very rare

histology: thin anastomosing

strands and cords of tumor cells

extending into dermis from

epidermis surrounded by

fibrous stroma

MELANOMA

BASAL CELL

CARCINOMA

MOHS

excision w/ 4 mm margins

EDC

XRT

imiquimod

topical 5-FU

photodynamic therapy,

cryosurgery

combination therapy: EDC +

imiquimod

MALIGNANT LESIONS

Gorlin Syndrome aka

Basal Cell Nevus

Syndrome

Hundreds of Basal Cells that

look like moles

Also get calcification of falx

cerebri, jaw cysts, bifid ribs

Auto dom

PATCH gene mutation

Kids

Excellent prognosis

erythematous, keratotic

papule or nodule

Metastases uncommon if

tumor < 1.5 cm deep

5% metastasize if 2 cm or

more and definite dermal

invasion

metastasizes usually to lung

Usually men

2nd MC skin cancer

Very rare in blacks

UVB > UVA exposure

transplant pts: need

frequent derm follow-up

other exposures: chronic

ulceration/inflammation,

scarring, arsenic from wells,

smoking

HPV 16/18

risk factors for metastasis:

ear/lip, impaired host, > 2 cm,

depth > 4 mm, perineural

invasion, poor differentiation

Irregular border

Indurated with

white/yellowish scale

Can see

hyperkeratosis/parakeratosis

Can see cells along the basal

layer are mildly irregular, some

are large w/ hyperchromatic

nuclei

Stay in bottom 1/3 of

epidermis

The dermis is bluish

keratin pearls

Surgical excision with

adequate margins

ELECTRODESICCATION AND

CURETTAGE (ED&C)

Excision: high risk (10 mm),

low risk (4 mm)

MOHS

Radiation-adjunctive therapy

Aldara-low cure rate

if palpable LN: fine

needle/surgical biopsy

Keratoacanthoma rapidly growing ulcerative

keratotic nodules that looks like

crater

GRYZBOWSKI SYNDROME:

multiple nonregressing,

generalized eruptive

FERGUSON SMITH

SYNDROME: familial,

spontaneously regressing

KERATOACANTHOMA

CENTRIFUGUM MARGINATUM:

solitary, expanding

erythematous plaque w/ central

regression. looks like discoid

elderly ~ 64 yo

more prevalent in Muir-

Torre syndrome pts

can spontaneously regress surgical excision: if regress

on own will heal w/ scarring

MTX injection, topical 5-FU,

imiquimod

radiation

Actinic Keratosis Very Common, precursor to

SCC that's confined to epidermis

mild erythema w/

imperceptible scale --> becomes

more papular and obvious later

cutaneous horns can overlie

AK

Caused by long term UV

exposure

sun-damaged skin on

balding scalp aka dermal

solar elastosis

Worse in transplant

patients

solar elastosis: greyish areas

in dermis

dysplastic cells in lower

epidermis, hyperkeratosis

need inspection and

palpation to detect, may be

imperceptible

LN2 (cryotherapy)

topical chemo like 5-FU or

Aldara

sunscreen

photodynamic therapy

BASAL CELL

CARCINOMA

SQUAMOUS

CELL

CARCINOMA

MALIGNANT LESIONS

Actinic Cheilitis diffuse AK/change of lip

loss of vermilion border

squamitization of mucosal tip

leukoplakia

SCC can arise from actinically

damaged tip --> can

metastasize in mouth and

spread to throat

Marjolins ulcer SCC coming from area of

scar/chronic inflammation

ulcer that doesn't heal

incisional biopsy

Bowen's Disease aka

SCC in Situ/

Erythrodysplasia of

Queyrat

Full thickness epidermal atypia

but not into the dermis

larger size, induration,

crusting, refractory to LN2 -->

BOWEN'S

can arise in non-sun exposed

sites

risk of progression to SCC

NOT invasive bc BM is intact

Dysplastic throughout

epidermis

LN2, topical chemo like 5-FU

or Aldara, or surgery. If on

genitalia, do MOHS

Leukoplakia MC premalignant lesion of the

oral mucosa, treat like SC-Cis

ddx = thrush, but this lesion

NON-SCRAPABLE

KARPOSI'S

SARCOMA

Spindle-cell tumor derived

from endothelium

Caused by Human

Herpesvirus 8 (HHV8) aka KSHV

bluish-red or purple bumps on

the skin (from vascular lesions

from epithelium)

Epidemic, AIDS-related

Immunocompromised

Classic or sporadic

Endemic (African)

irregularly diliated

anastomosing vascular

channels

HPV associated large well-differentiated nests

of eosinophilic keratinocyts w/

"pushing border"

Oral florid

papillomatosis

mouth

Giant condylomata of

Buschke-Lwenstein

on genitalia

Epithelioma

cuniculatum (plantar

surface of the foot)

on plantar foot

SQUAMOUS

CELL

CARCINOMA

VERRUCOUS

CARCINOMA SurgeryDO NOT

Radiatethis will only piss

them off and they will turn

deeply invasive

MALIGNANT LESIONS

Mycosis Fungoides (T-

Cell) Pts are commonly

misdiagnosed with eczema

plaque stage: looks like

eczema, but steroids don't

work

tumor stage: knee picture.

Looks pretty bad

Sezary Syndrome Leukemic form of Mycosis

Fungoides

high mortality rate

Paget's of Breast Extension of underlying ductal

carcinoma to the skin including

the nipple, and areola

Similar to Bowens dz

Surgery

Extramammary

Paget's

MC labia majora

Associated with underlying

malignancy 20% of the time ->

most common is rectal, bladder,

renal, uterine

If you see a lesion and its

associated with an internal

cancer, 50% have already

metastasized

F>M

XERODERMA

PIGMENTOSUM

early onset of disease states:

1000x risk of skin cancers

defect in nucleotide excision

repair genes--> exaggerated

response to UV

RECESSIVE

DYSTROPHIC EB

basement membrane familial

disease: skin sloughs off easily

and SCC develops in scars or

sites of chronic irritation

collagen type VII defect

leading cause of death

beyond childhood in pts w/

dystrophic EB --> septic

SCC occurs on extremities

and metastasizes early

BAZEX

SYNDROME

early onset BCC

follicular atrophoderma

congenital hypotrichosis: loss

of eyebrows and hair

ROMBO

SYNDROME

early onset BCC

peripheral vasodilation w/

cyanosis

hypotrichosis

milium/cysts

blepharitis

EPIDERMO-

DYSPLASIA

VERRUCIFORMIS

flat wart-like lesions in early

childhood --> acutally SCCHPV 3, 5, 8

OCULO-

CUTANEOUS

ALBINISM

pigment disorder of eyes, hair,

skin

no melanin --> no UV

protection --> inc SCC,

melanomas > BCC

PRIMARY

CUTANEOUS

LYMPHOMAS

PAGET DISEASE

UV protection

Derm Pathology

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